5 Emergency Craniotomy

Michael V. Presta and Ricky B. Shah

KEY POINTS

1. Prevention of aggravating factors that worsen secondary injury is the mainstay of perioperative care for patients with traumatic brain injury.

2. Succinylcholine is not contraindicated with patients with intracranial hypertension as human studies have not shown demonstrable increases in ICP, especially if the patient has adequate PaCO₂, MAP, and depth of anesthesia.

3. Recommendations by the Brain Trauma Foundation are a cerebral perfusion pressure (MAP − ICP) goals of 50 to 70 mm Hg.

4. Treatment of intracranial hypertension should include enabling venous drainage, diuretic therapy, barbiturates, propofol, and extraventricular drain. Hyperventilation should be used only in short periods of time to quickly and effectively decrease ICP. New data has put decompressive craniectomy into question.

5. Normoglycemia and normothermia should be strived for in caring for these patients in the operating room.

EMERGENCY CRANIOTOMY for neurologic conditions caused by entities such as traumatic brain injury (TBI) and its sequelae involves complex and difficult management decisions. According to the National Center for Injury Prevention and Control, TBI is the leading injury cause of death and permanent disability worldwide. In the United States alone, 1.6 million cases of TBI present to emergency services every year [1]. Many more cases go unreported and untreated. These TBIs lead to more than 250,000 hospitalizations and, ultimately, 50,000 deaths [2]. Treatment of patients with TBI begins at the time of impact. The decision to operate depends mainly on the patient’s neurologic status, imaging findings, and extent of cranial injury. Many of these critically ill patients have multiple injuries resulting in significant hemodynamic alterations. As a result, team members from anesthesia play a crucial role throughout the perioperative course and ultimate outcome.

I. Epidemiology. TBIs affect all patient populations regardless of race, gender, or age. They occur in a bimodal fashion between the adolescent ages of 15 and 24 and again at age 75 or older. In all age groups, males are affected two times more often than females. The most common causes of TBIs in the United States are motor vehicle collisions, violence, and falls [3–5].

II. Classification of head injury

A. Primary injury (irreversible impact damage) manifests within milliseconds and occurs before the patient arrives at the hospital. These include skull fractures, epidural and subdural hemorrhage, vascular bleeds, subarachnoid bleeds, cortical contusions, bone fragmentations, lacerations, and brainstem contusions. The primary injury may be focal or diffuse. Focal injuries comprise the traumatic intracranial hematomas and contusions; while concussion and diffuse axonal injury are the components of diffuse injury [6,7].

1. Skull fractures may be of three categories. Linear fractures, depressed fractures, and penetrating or perforating injuries. This type of injury is related to the nature of the impact. Definite evidence of dural penetration, and/or +/− neurologic deficit usually signals urgent need for craniotomy [8].

2. Epidural hematomas (EDH) located between the skull and dura, are almost always caused by skull fractures. Most occur in the temporoparietal region as skull fractures crossing the path of the middle meningeal artery [9].

a. Incidence. 1% of head trauma admissions (=50% the incidence of acute subdurals) usually occurs in young male adults, and is rare before the age of 2 years or after 60 years.

b. Presentation. Is seen as a “textbook” presentation of a brief posttraumatic loss of consciousness followed by a “lucid interval” for several hours, then obtundation, contralateral hemiparesis, and ipsilateral papillary dilation.

c. Emergent treatment. Emergent craniotomy and surgical evacuation for any symptomatic EDH or any asymptomatic EDH >1 cm in its thickest measurement. Threshold for pediatric patients is even lower as these patients do not have the room adult patients have to reabsorb the blood and for clot to initiate [10,11].

3. Acute subdural hematomas (ASDHs) are insidiously developing crescent-shaped focal intracranial lesions frequently caused by the tearing of bridging veins connecting the cerebral cortex and dural sinuses. This is a consequence seen in sudden movements of the head often seen in falls, assaults, and acceleration–deceleration events from sudden motor vehicle collisions. The magnitude of impact damage is usually much higher in ASDHs than in EDHs, which generally makes this lesion more lethal.

a. Incidence. ASDHs have been reported to occur in 5% to 25% of patients with severe head injuries, depending on the study. Chronic SDH has been reported to be 1 to 5.3 cases per 100,000 people per year. Anticoagulation, such as with heparin or warfarin (Coumadin), may be a contributing factor. ASDHs are usually characterized based on their size, location, and age (i.e., whether they are acute, subacute, or chronic). These factors, as well as the neurologic and medical conditions of the patient, determine the course of treatment and may also influence the outcome. ASDHs are usually caused by trauma but can be spontaneous or caused by a procedure, such as a lumbar puncture [12].

b. Presentation. Severe underlying primary brain injury with often no “lucid interval.” A host of findings could be associated with these, such as brisk or abnormal reflexes, aphasia (usually with a left-sided hematoma), upper-extremity drift, or impairment of cortical sensory function.

1

c. Emergent treatment. Rapid surgical evacuation via craniotomy or burr holes should be considered for symptomatic subdurals that are greater than about 1 cm at the thickest point (or >5 mm in peds). Smaller subdurals often do not require evacuation, and surgery may increase the brain injury if there is severe hemispheric swelling with herniation through the craniotomy [13].

1

4. Intracerebral hematoma (ICH). ICH is a common cause of stroke, trailing only embolic infarction and atherosclerotic thrombosis in frequency. When it occurs, ICH is a medical emergency, characterized by high morbidity and mortality, which should be promptly diagnosed and aggressively managed. Hematoma expansion and early deterioration are common within the first few hours after onset. The risk for early neurologic deterioration and the high rate of poor long-term outcomes underscore the need for aggressive early management. Hypertensive hemorrhages occur in the territory of penetrator arteries that branch off major intracerebral arteries, often at 90-degree angles with the parent vessel. The blood vessels that give rise to hypertensive hemorrhage generally are the same as those affected by hypertensive occlusive disease and diabetic vasculopathy. Thus typical locations of hypertensive ICH are putamen, subcortical cerebral lobe, thalamus, cerebellum, brainstem, and caudate nucleus. Each location may differ in clinical presentation, prognosis, and consideration for surgical treatment. Noncontrast cranial CT is the study of choice to evaluate for the presence of acute ICH, which is evident almost immediately. CT scans define the size and location of the hematoma. They also provide information about extension into the ventricular system, the presence of surrounding edema, and shifts in brain contents (hernia). The decision about whether and when to surgically remove ICH remains controversial. The pathophysiology of brain injury surrounding the hematoma is due to the mechanical effects of the growing mass of blood as well as the subsequent toxic effects of blood in the surrounding brain tissue. Early surgery to limit the mechanical compression of brain and the toxic effects of blood may limit injury, but the surgical risks in a patient with ongoing bleeding may be greater. In addition, operative removal of hemorrhage by craniotomy in all but the most superficial hemorrhages involves cutting through uninjured brain. Even after the International Surgical Trial in Intracerebral Haemorrhage (STICH) published its results from over an 8-year period, drawing firm conclusions from the data is a difficult and daunting task. Among the limitations of ICH surgical trials is that young and middle-aged patients at risk of herniation from large ICHs were unlikely to be randomized for treatment. The American Stroke Association (ASA) 2010 guidelines recommend patients with cerebellar hemorrhage who are deteriorating neurologically or who have brainstem compression and/or hydrocephalus from ventricular obstruction should undergo surgical removal of the hemorrhage as soon as possible. Initial treatment of these patients with ventricular drainage alone rather than surgical evacuation is not recommended. For patients presenting with lobar clots >30 mL and within 1 cm of the surface, evacuation of supratentorial ICH by standard craniotomy might be considered. Although theoretically attractive, no clear evidence at present indicates that ultra-early removal of supratentorial ICH improves functional outcome or mortality rate. Very early craniotomy in these patients may be harmful due to increased risk of recurrent bleeding [14,15].

1

B. Secondary injury develops (minutes to hours) subsequent to the impact damage. It includes a constellation of complicating injuries from the inciting event and consists of intracranial hematomas, edema, hypoxia, ischemia (primarily due to elevated intracranial pressure [ICP]), and/or shock. Prevention of further hypoxemia, hypotension, hypercarbia, anemia, and hyperglycemia are the mainstay of managing further injury.

1

III. Preoperative evaluation and preparation

A. Neurologic assessment

1. The Glasgow coma scale (GCS) is the most widely used method to assess neurologic status and severity of brain dysfunction following head trauma [16

Only gold members can continue reading. Log In or Register to continue